Since BCR signaling is thought to induce NFAT activity through a PLCγ2 pathway, and the ability of BCR signaling to reactivate EBV in Akata virus-infected Burkitt lymphoma cells requires both BTK and PKC activity [48,49,51,52], we also compared the effect of PLCγ, BTK and PKC inhibitors on the amount of constitutive lytic Z expression in BL5 cells versus Mutu cells. Here, BTK is linked to Burkitt lymphoma.